Problem 12
Although both hexokinase and phosphofructokinase catalyze irreversible steps in glycolysis and the hexokinase-catalyzed step is first, phosphofructokinase is nonetheless the pacemaker of glycolysis. What does this information tell you about the fate of the glucose 6 -phosphate formed by hexokinase?
Problem 13
Why is the regulation of phosphofructokinase by energy charge not as important in the liver as it is in muscle?
Problem 14
. Why can't the reactions of the glycolytic pathway simply be run in reverse to synthesize glucose?
Problem 15
What are the principle fates of pyruvate generated in glycolysis?
Problem 17
Why is it in the muscle's best interest to export lactic acid into the blood during intense exercise?
Problem 18
Describe the pathways by which fructose is prepared for entry into glycolysis.
Problem 19
. Suppose that an obligate anaerobe suffered a mutation that resulted in the loss of triose phosphate isomerase activity. How would this loss affect the ATP yield of fermentation? Could such an organism survive?
Problem 22
The intravenous infusion of fructose into healthy volunteers leads to a two- to five fold increase in the level of lactate in the blood, a far greater increase than that observed after the infusion of the same amount of glucose. (a) Why is glycolysis more rapid after the infusion of fructose? (b) Fructose has been used in place of glucose for intravenous feeding. Why is this use of fructose unwise?
Problem 23
Arsenate \(\left(\mathrm{AsO}_{4}^{3-}\right)\) closely resembles \(P_{i}\) in structure and reactivity. In the reaction catalyzed by glyceraldehyde 3 -phosphate dehydrogenase, arsenate can replace phosphate in attacking the energy-rich thioester intermediate. The product of this reaction, 1 -arseno3-phosphoglycerate, is unstable. It and other acyl arsenates are rapidly and spontaneously hydrolyzed. What is the effect of arsenate on energy generation in a cell?
Problem 24
In the conversion of glucose into two molecules of lactate, the NADH generated earlier in the pathway is oxidized to \(\mathrm{NAD}^{+} .\) Why is it not to the cell's advantage to simply make more \(\mathrm{NAD}^{+}\) so that the regeneration would not be necessary? After all, the cell would save much energy because it would no longer need to synthesize lactic acid dehydrogenase.
